Taubes: What Really Makes Us Fat
Investigative science journalist Gary Taubes writes in The New York Times about the results of a clinical trial by Dr. David Ludwig and colleagues from Boston Children’s Hospital:
What was done by Dr. Ludwig’s team has never been done before. First they took obese subjects and effectively semi-starved them until they’d lost 10 to 15 percent of their weight. Such weight-reduced subjects are particularly susceptible to gaining the weight back. Their energy expenditure drops precipitously and they burn fewer calories than people who naturally weigh the same. This means they have to continually fight their hunger just to maintain their weight loss. The belief is that weight loss causes “metabolic adaptations,” which make it almost inevitable that the weight will return. Dr. Ludwig’s team then measured how many calories these weight-reduced subjects expended daily, and that’s how many they fed them. But now the subjects were rotated through three very different diets, one month for each. They ate the same amount of calories on all three, equal to what they were expending after their weight loss, but the nutrient composition of the diets was very different.
One diet was low-fat and thus high in carbohydrates. This was the diet we’re all advised to eat: whole grains, fruits, vegetables, lean sources of protein. One diet had a low glycemic index: fewer carbohydrates in total, and those that were included were slow to be digested — from beans, non-starchy vegetables and other minimally processed sources. The third diet was Atkins, which is very low in carbohydrates and high in fat and protein.
The results were remarkable. Put most simply, the fewer carbohydrates consumed, the more energy these weight-reduced people expended. On the very low-carbohydrate Atkins diet, there was virtually no metabolic adaptation to the weight loss. These subjects expended, on average, only 100 fewer calories a day than they did at their full weights. Eight of the 21 subjects expended more than they did at their full weights — the opposite of the predicted metabolic compensation.
On the very low-carbohydrate diet, Dr. Ludwig’s subjects expended 300 more calories a day than they did on the low-fat diet and 150 calories more than on the low-glycemic-index diet. As Dr. Ludwig explained, when the subjects were eating low-fat diets, they’d have to add an hour of moderate-intensity physical activity each day to expend as much energy as they would effortlessly on the very-low-carb diet. And this while consuming the same amount of calories. If the physical activity made them hungrier — a likely assumption — maintaining weight on the low-fat, high-carb diet would be even harder. Why does this speak to the very cause of obesity? One way to think about this is to consider weight-reduced subjects as “pre-obese.” They’re almost assuredly going to get fatter, and so they can be research stand-ins — perhaps the best we have — for those of us who are merely predisposed to get fat but haven’t done so yet and might take a few years or decades longer to do it.
If we think of Dr. Ludwig’s subjects as pre-obese, then the study tells us that the nutrient composition of the diet can trigger the predisposition to get fat, independent of the calories consumed. The fewer carbohydrates we eat, the more easily we remain lean. The more carbohydrates, the more difficult. In other words, carbohydrates are fattening, and obesity is a fat-storage defect. What matters, then, is the quantity and quality of carbohydrates we consume and their effect on insulin.
From this perspective, the trial suggests that among the bad decisions we can make to maintain our weight is exactly what the government and medical organizations like the American Heart Association have been telling us to do: eat low-fat, carbohydrate-rich diets, even if those diets include whole grains and fruits and vegetables.
And let’s repeat from the piece, and as Taubes laid out in these books, and as I’ve been posting on the basis of for much of this decade:
In other words, carbohydrates are fattening, and obesity is a fat-storage defect. What matters, then, is the quantity and quality of carbohydrates we consume and their effect on insulin.